LIFE01200604005 Shri Somnath Ghosh - Homi Bhabha National ...

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CHAPTER 5 REFERENCES [35] Nghiem, P.; Park, P. K.; Kim, Y.; Vaziri, C.; Schreiber, S. L. ATR inhibition selectively sensitizes G1 checkpoint-deficient cells to lethal premature chromatin condensation. Proc Natl Acad Sci U S A 98:9092-9097; 2001. [36] Cha, R. S.; Kleckner, N. ATR homolog Mec1 promotes fork progression, thus averting breaks in replication slow zones. Science 297:602-606; 2002. [37] O'Driscoll, M.; Ruiz-Perez, V. L.; Woods, C. G.; Jeggo, P. A.; Goodship, J. A. A splicing mutation affecting expression of ataxia-telangiectasia and Rad3-related protein (ATR) results in Seckel syndrome. Nat Genet 33:497-501; 2003. [38] Tibbetts, R. S.; Cortez, D.; Brumbaugh, K. M.; Scully, R.; Livingston, D.; Elledge, S. J.; Abraham, R. T. Functional interactions between BRCA1 and the checkpoint kinase ATR during genotoxic stress. Genes Dev 14:2989-3002; 2000. [39] Dodson, G. E.; Shi, Y.; Tibbetts, R. S. DNA replication defects, spontaneous DNA damage, and ATM-dependent checkpoint activation in replication protein A- deficient cells. J Biol Chem 279:34010-34014; 2004. [40] Bomgarden, R. D.; Yean, D.; Yee, M. C.; Cimprich, K. A. A novel protein activity mediates DNA binding of an ATR-ATRIP complex. J Biol Chem 279:13346- 13353; 2004. [41] Stiff, T.; Reis, C.; Alderton, G. K.; Woodbine, L.; O'Driscoll, M.; Jeggo, P. A. Nbs1 is required for ATR-dependent phosphorylation events. Embo J 24:199-208; 2005. [42] Busino, L.; Donzelli, M.; Chiesa, M.; Guardavaccaro, D.; Ganoth, D.; Dorrello, N. V.; Hershko, A.; Pagano, M.; Draetta, G. F. Degradation of Cdc25A by beta-TrCP during S phase and in response to DNA damage. Nature 426:87-91; 2003. 217
CHAPTER 5 REFERENCES [43] Jin, J.; Shirogane, T.; Xu, L.; Nalepa, G.; Qin, J.; Elledge, S. J.; Harper, J. W. SCFbeta-TRCP links Chk1 signaling to degradation of the Cdc25A protein phosphatase. Genes Dev 17:3062-3074; 2003. [44] Heffernan, T. P.; Simpson, D. A.; Frank, A. R.; Heinloth, A. N.; Paules, R. S.; Cordeiro-Stone, M.; Kaufmann, W. K. An ATR- and Chk1-dependent S checkpoint inhibits replicon initiation following UVC-induced DNA damage. Mol Cell Biol 22:8552-8561; 2002. [45] Bartek, J.; Lukas, C.; Lukas, J. Checking on DNA damage in S phase. Nat Rev Mol Cell Biol 5:792-804; 2004. [46] Andreassen, P. R.; D'Andrea, A. D.; Taniguchi, T. ATR couples FANCD2 monoubiquitination to the DNA-damage response. Genes Dev 18:1958-1963; 2004. [47] Wang, X.; D'Andrea, A. D. The interplay of Fanconi anemia proteins in the DNA damage response. DNA Repair (Amst) 3:1063-1069; 2004. [48] Venkitaraman, A. R. Tracing the network connecting BRCA and Fanconi anaemia proteins. Nat Rev Cancer 4:266-276; 2004. [49] Pichierri, P.; Rosselli, F. The DNA crosslink-induced S-phase checkpoint depends on ATR-CHK1 and ATR-NBS1-FANCD2 pathways. Embo J 23:1178-1187; 2004. [50] Tibbetts, R. S.; Brumbaugh, K. M.; Williams, J. M.; Sarkaria, J. N.; Cliby, W. A.; Shieh, S. Y.; Taya, Y.; Prives, C.; Abraham, R. T. A role for ATR in the DNA damageinduced phosphorylation of p53. Genes Dev 13:152-157; 1999. [51] Lakin, N. D.; Hann, B. C.; Jackson, S. P. The ataxia-telangiectasia related protein ATR mediates DNA-dependent phosphorylation of p53. Oncogene 18:3989-3995; 1999. 218
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RADIATION INDUCED SIGNALING IN MAMM
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DECLARATION I, hereby declare that
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CONTENTS Page No. SYNOPSIS………
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2.11 Measurement of NO production
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PREAMBLE SYNOPSIS Ionising radiatio
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SYNOPSIS Aims and Objectives: To St
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SYNOPSIS 2.6 Immunofluorescence sta
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SYNOPSIS ATM gene expression, which
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SYNOPSIS Percentage Survival 100 80
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SYNOPSIS Ratio of Rad52 to Actin Ra
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Relative Phosphorylation 45 40 35 3
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SYNOPSIS Fig. 3.3A Clonogenic Cell
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SYNOPSIS (A) Av No. of phospho BRCA
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SYNOPSIS Percentage Survival 120 10
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SYNOPSIS Fig.3.4B. Existance of cro
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SYNOPSIS Fig. 3.4EDNA damage in EL-
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SYNOPSIS subsequent cytotoxicity ca
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SYNOPSIS [4] Hall, E. J. Radiobiolo
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CHAPTER 1 INTRODUCTION INTRODUCTION
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CHAPTER 1 INTRODUCTION 15.8% 9.56%
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CHAPTER 1 INTRODUCTION far apart an
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CHAPTER 1 INTRODUCTION and are more
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CHAPTER 1 INTRODUCTION 1.3 DNA dama
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CHAPTER 1 INTRODUCTION associates w
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CHAPTER 1 INTRODUCTION are unable t
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CHAPTER 1 INTRODUCTION Perhaps one
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CHAPTER 1 INTRODUCTION occurs at DS
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CHAPTER 1 INTRODUCTION related prot
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CHAPTER 1 INTRODUCTION damage must
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CHAPTER 1 INTRODUCTION At the prese
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CHAPTER 1 INTRODUCTION predominant
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CHAPTER 1 INTRODUCTION provide a me
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CHAPTER 1 INTRODUCTION hypersensiti
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CHAPTER 1 INTRODUCTION cycle-specif
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CHAPTER 1 INTRODUCTION 1.4 Overview
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CHAPTER 1 INTRODUCTION 1.4.1 Radiat
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CHAPTER 1 INTRODUCTION interaction
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CHAPTER 1 INTRODUCTION p90S6 kinase
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CHAPTER 1 INTRODUCTION CD4 (formerl
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CHAPTER 1 INTRODUCTION unrepaired d
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CHAPTER 1 INTRODUCTION well to the
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CHAPTER 1 INTRODUCTION 1.6 Radiatio
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CHAPTER 1 INTRODUCTION becomes pote
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CHAPTER 2 MATERIALS AND METHODS MAT
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CHAPTER 2 MATERIALS AND METHODS 2.2
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CHAPTER 2 MATERIALS AND METHODS res
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CHAPTER 2 MATERIALS AND METHODS Arr
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CHAPTER 2 MATERIALS AND METHODS PBS
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CHAPTER 2 MATERIALS AND METHODS the
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CHAPTER 2 MATERIALS AND METHODS 2.1
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CHAPTER 3 RESULTS RESULTS 93
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CHAPTER 3 RESULTS fractionated regi
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CHAPTER 3 RESULTS On comparison of
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CHAPTER 3 RESULTS Table 3.1.2A List
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CHAPTER 3 RESULTS 80 NM_002185 IL7R
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CHAPTER 3 RESULTS SAA2 149 AU134977
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CHAPTER 3 RESULTS 221 LOC643167 RNA
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CHAPTER 3 RESULTS 299 BF244402 FBXO
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CHAPTER 3 RESULTS CDK4) 57 AU152107
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CHAPTER 3 RESULTS 134 AL045793 METT
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CHAPTER 3 RESULTS 58 AF237813 ABAT
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CHAPTER 3 RESULTS 127 AI809749 ORMD
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CHAPTER 3 RESULTS 31 BE615699 UNC84
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CHAPTER 3 RESULTS 47 AF026303 SULT1
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CHAPTER 3 RESULTS 117 BF062193 CYor
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CHAPTER 3 RESULTS 187 AL036662 ---
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CHAPTER 3 RESULTS 52 AV686514 EMP2
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CHAPTER 3 RESULTS exposed to 10 Gy
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CHAPTER 3 RESULTS Fig.3.1.4 Gene ex
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CHAPTER 3 RESULTS Fig. 3.1.6 Radiat
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CHAPTER 3 RESULTS Fig. 3.1.7 Transl
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CHAPTER 3 RESULTS 3.1.9 Stabilizati
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CHAPTER 3 RESULTS 23±1.5% (Fig. 3.
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CHAPTER 3 RESULTS whereas only the
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CHAPTER 3 RESULTS with equal doses
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CHAPTER 3 RESULTS Fig.3.3.1.2 Forma
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CHAPTER 3 RESULTS Fig.3.3.1.3 Phosp
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CHAPTER 3 RESULTS (7.5±0.64) (Fig.
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CHAPTER 3 RESULTS Fig.3.3.1.7b Phos
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CHAPTER 3 RESULTS 3.3.2 Oxygen beam
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CHAPTER 3 RESULTS in all the cells.
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CHAPTER 3 RESULTS 3.3.2.3 Radiation
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Page 176 and 177: CHAPTER 3 RESULTS Fig.3.3.2.7 Apopt
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Page 190 and 191: CHAPTER 3 RESULTS Fig.3.4.4b DNA da
Page 192 and 193: CHAPTER 3 RESULTS Fig.3.4.5a Gene e
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Page 216 and 217: CHAPTER 4 DISCUSSION Numerous studi
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Page 220 and 221: CHAPTER 4 DISCUSSION The survival o
Page 222 and 223: CHAPTER 5 REFERENCES [1] Khan, F. T
Page 224 and 225: CHAPTER 5 REFERENCES [19] Woo, R. A
Page 228 and 229: CHAPTER 5 REFERENCES [52] McKay, B.
Page 230 and 231: CHAPTER 5 REFERENCES [69] Cary, R.
Page 232 and 233: CHAPTER 5 REFERENCES [84] Uziel, T.
Page 234 and 235: CHAPTER 5 REFERENCES [98] Liu, Y.;
Page 236 and 237: CHAPTER 5 REFERENCES [111] Fei, P.;
Page 238 and 239: CHAPTER 5 REFERENCES [127] Frank, K
Page 240 and 241: CHAPTER 5 REFERENCES [141] Pierce,
Page 242 and 243: CHAPTER 5 REFERENCES [156] Roots, R
Page 244 and 245: CHAPTER 5 REFERENCES [171] Xia, Z.;
Page 246 and 247: CHAPTER 5 REFERENCES (MAP) kinase c
Page 248 and 249: CHAPTER 5 REFERENCES phosphorylatio
Page 250 and 251: CHAPTER 5 REFERENCES [211] Anderson
Page 252 and 253: CHAPTER 5 REFERENCES [229] Konca, K
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Page 256 and 257: CHAPTER 5 REFERENCES [261] Miralbel
Page 258 and 259: CHAPTER 5 REFERENCES [278] Weizman,
Page 260 and 261: CHAPTER 5 REFERENCES [294] Zhou, H.
Page 262 and 263: PUBLICATIONS AND PRESENTATIONS Publ
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Mutation Research 716 (2011) 10-19
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Mutation Research 723 (2011) 190-19
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Cancer Invest Downloaded from infor
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